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Journal articles on the topic 'Mitochondrial biogenesis markers'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Mesbah Moosavi, Zahra S., and David A. Hood. "The unfolded protein response in relation to mitochondrial biogenesis in skeletal muscle cells." American Journal of Physiology-Cell Physiology 312, no. 5 (2017): C583—C594. http://dx.doi.org/10.1152/ajpcell.00320.2016.

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Mitochondria comprise both nuclear and mitochondrially encoded proteins requiring precise stoichiometry for their integration into functional complexes. The augmented protein synthesis associated with mitochondrial biogenesis results in the accumulation of unfolded proteins, thus triggering cellular stress. As such, the unfolded protein responses emanating from the endoplasmic reticulum (UPRER) or the mitochondrion (UPRMT) are triggered to ensure correct protein handling. Whether this response is necessary for mitochondrial adaptations is unknown. Two models of mitochondrial biogenesis were us

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Jun, Lauren, Emily Knight, Tom L. Broderick, et al. "Moderate-Intensity Exercise Enhances Mitochondrial Biogenesis Markers in the Skeletal Muscle of a Mouse Model Affected by Diet-Induced Obesity." Nutrients 16, no. 12 (2024): 1836. http://dx.doi.org/10.3390/nu16121836.

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Skeletal muscle is composed of bundles of muscle fibers with distinctive characteristics. Oxidative muscle fiber types contain higher mitochondrial content, relying primarily on oxidative phosphorylation for ATP generation. Notably, as a result of obesity, or following prolonged exposure to a high-fat diet, skeletal muscle undergoes a shift in fiber type toward a glycolytic type. Mitochondria are highly dynamic organelles, constantly undergoing mitochondrial biogenesis and dynamic processes. Our study aims to explore the impact of obesity on skeletal muscle mitochondrial biogenesis and dynamic

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Zou, Peng, Longhua Liu, Louise D. Zheng, et al. "Coordinated Upregulation of Mitochondrial Biogenesis and Autophagy in Breast Cancer Cells: The Role of Dynamin Related Protein-1 and Implication for Breast Cancer Treatment." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/4085727.

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Overactive mitochondrial fission was shown to promote cell transformation and tumor growth. It remains elusive how mitochondrial quality is regulated in such conditions. Here, we show that upregulation of mitochondrial fission protein, dynamin related protein-1 (Drp1), was accompanied with increased mitochondrial biogenesis markers (PGC1α, NRF1, and Tfam) in breast cancer cells. However, mitochondrial number was reduced, which was associated with lower mitochondrial oxidative capacity in breast cancer cells. This contrast might be owing to enhanced mitochondrial turnover through autophagy, bec

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Sun, Qi, Alejandro Bravo Iniguez, Qiyu Tian, Min Du та Mei-Jun Zhu. "PGC-1α Is Indispensable in Purple Potato Promoted Intestinal Epithelial Differentiation and Mitochondrial Biogenesis". Current Developments in Nutrition 6, Supplement_1 (2022): 537. http://dx.doi.org/10.1093/cdn/nzac077.040.

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Abstract Objectives Purple potato (PP) is a good dietary source of polyphenol and promotes gut epithelial health. The objective of this study is to examine the impact of PP extract on mitochondrial biogenesis and evaluate the role of peroxisome proliferator-activated receptor gamma coactivator (PGC)-1α in this. Methods In cultured colonic epithelial Caco-2 cells, the effects of PP extract on PGC-1α, cell differentiation, and markers of mitochondrial biogenesis, including mitochondrial DNA content, mitochondrial enzyme gene expression, and levels of metabolic intermediates, were first evaluated

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Jin, Sun Woo, Gi Ho Lee, Ji Yeon Kim, et al. "Effect of Porcine Whole Blood Protein Hydrolysate on Slow-Twitch Muscle Fiber Expression and Mitochondrial Biogenesis via the AMPK/SIRT1 Pathway." International Journal of Molecular Sciences 23, no. 3 (2022): 1229. http://dx.doi.org/10.3390/ijms23031229.

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Skeletal muscle is a heterogeneous tissue composed of a variety of functionally different fiber types. Slow-twitch type I muscle fibers are rich with mitochondria, and mitochondrial biogenesis promotes a shift towards more slow fibers. Leucine, a branched-chain amino acid (BCAA), regulates slow-twitch muscle fiber expression and mitochondrial function. The BCAA content is increased in porcine whole-blood protein hydrolysates (PWBPH) but the effect of PWBPH on muscle fiber type conversion is unknown. Supplementation with PWBPH (250 and 500 mg/kg for 5 weeks) increased time to exhaustion in the

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Joe, Yeonsoo, Min Zheng, Hyo Jeong Kim, et al. "Cilostazol attenuates murine hepatic ischemia and reperfusion injury via heme oxygenase-dependent activation of mitochondrial biogenesis." American Journal of Physiology-Gastrointestinal and Liver Physiology 309, no. 1 (2015): G21—G29. http://dx.doi.org/10.1152/ajpgi.00307.2014.

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Hepatic ischemia-reperfusion (I/R) can cause hepatocellular injury associated with the inflammatory response and mitochondrial dysfunction. We studied the protective effects of the phosphodiesterase inhibitor cilostazol in hepatic I/R and the roles of mitochondria and the Nrf2/heme oxygenase-1 (HO-1) system. Wild-type, Hmox1 −/−, or Nrf2 −/− mice were subjected to hepatic I/R in the absence or presence of cilostazol followed by measurements of liver injury. Primary hepatocytes were subjected to cilostazol with the HO-1 inhibitor ZnPP, or Nrf2-specific siRNA, followed by assessment of mitochond

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Tedesco, Laura, Fabio Rossi, Chiara Ruocco, et al. "Experimental evidence on the efficacy of two new metabolic modulators on mitochondrial biogenesis and function in mouse cardiomyocytes." Journal of Population Therapeutics and Clinical Pharmacology 27, SP2 (2020): e12-e21. http://dx.doi.org/10.15586/jptcp.v27isp2.740.

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Proper maintenance of mitochondrial homeostasis is essential for cell health, and mitochondrial dysfunction underlies several metabolic and heart diseases. Stimulation of mitochondrial biogenesis represents a valuable therapeutic tool for the prevention and treatment of disorders characterized by a deficit in energy metabolism. The present study aimed to potentiate the mitochondrial biogenetic efficacy of an amino acid (AA) mixture, enriched in branched-chain amino acids (BCAAs), which we previously showed to boost mitochondrial biogenesis, leading to life span extension and reducing of muscle

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Prieto-Carrasco, Rodrigo, Fernando E. García-Arroyo, Omar Emiliano Aparicio-Trejo, et al. "Progressive Reduction in Mitochondrial Mass Is Triggered by Alterations in Mitochondrial Biogenesis and Dynamics in Chronic Kidney Disease Induced by 5/6 Nephrectomy." Biology 10, no. 5 (2021): 349. http://dx.doi.org/10.3390/biology10050349.

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The five-sixth nephrectomy (5/6Nx) model is widely used to study the mechanisms involved in chronic kidney disease (CKD) progression. Mitochondrial impairment is a critical mechanism that favors CKD progression. However, until now, there are no temporal studies of the change in mitochondrial biogenesis and dynamics that allow determining the role of these processes in mitochondrial impairment and renal damage progression in the 5/6Nx model. In this work, we determined the changes in mitochondrial biogenesis and dynamics markers in remnant renal mass from days 2 to 28 after 5/6Nx. Our results s

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Wang, Yang, Zhijiang Chen, Yu Zhang, Suzhen Fang, and Qiyi Zeng. "Mitochondrial biogenesis of astrocytes is increased under experimental septic conditions." Chinese Medical Journal 127, no. 10 (2014): 1837–42. http://dx.doi.org/10.3760/cma.j.issn.0366-6999.20131934.

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Background Mitochondrial dysfunction has been reported to be one of the contributing factors of sepsis-associated encephalopathy (SAE). Mitochondrial biogenesis controls mitochondrial homeostasis and responds to changes in cellular energy demand. In addition, it is enhanced or decreased due to mitochondrial dysfunction during SAE. The aim of this study was to explore the changes of mitochondrial biogenesis of astrocytes under septic conditions. Methods Lipopolysaccharide (LPS; 50 ng/ml) and interferon-γ (IFN-γ; 200 U/ml) were incubated with astrocytes to model the effects of a septic insult on

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Sheldon, Ryan D., Grace M. Meers, E. Matthew Morris, et al. "eNOS deletion impairs mitochondrial quality control and exacerbates Western diet-induced NASH." American Journal of Physiology-Endocrinology and Metabolism 317, no. 4 (2019): E605—E616. http://dx.doi.org/10.1152/ajpendo.00096.2019.

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Dysregulated mitochondrial quality control leads to mitochondrial functional impairments that are central to the development and progression of hepatic steatosis to nonalcoholic steatohepatitis (NASH). Here, we identify hepatocellular localized endothelial nitric oxide synthase (eNOS) as a novel master regulator of mitochondrial quality control. Mice lacking eNOS were more susceptible to Western diet-induced hepatic inflammation and fibrosis in conjunction with decreased markers of mitochondrial biogenesis and turnover. The hepatocyte-specific influence was verified via magnetic activated cell

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Uche, Nnamdi, Qiang Dai, Shuping Lai, and Ivor Benjamin. "20902 Elucidation of Cardioprotective Mechanisms via Human Models of Chemotherapy-Induced Cardiotoxicity." Journal of Clinical and Translational Science 5, s1 (2021): 1. http://dx.doi.org/10.1017/cts.2021.404.

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ABSTRACT IMPACT: This work should provide further insights to mechanisms of the negative consequences of chemotherapy drugs, specifically in the cardiovascular system. OBJECTIVES/GOALS: Cardiotoxicity remains a safety concern in the development or utilization of chemotherapeutics largely due to the gap in knowledge of the mechanisms of toxicity. The pathophysiology of this cardiotoxicity has not been fully elucidated but data from our lab as well as other recent studies hint toward implications of mitochondrial (mito) biogenesis. METHODS/STUDY POPULATION: Prophylactic use of the beta-blocker c

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Stevanović-Silva, Jelena, Jorge Beleza, Pedro Coxito, Paulo J. Oliveira, António Ascensão, and José Magalhães. "Gestational Exercise Antagonises the Impact of Maternal High-Fat High-Sucrose Diet on Liver Mitochondrial Alterations and Quality Control Signalling in Male Offspring." International Journal of Environmental Research and Public Health 20, no. 2 (2023): 1388. http://dx.doi.org/10.3390/ijerph20021388.

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Maternal high-caloric nutrition and related gestational diabetes mellitus (GDM) are relevant modulators of the intrauterine environment, increasing the risk of liver metabolic alterations in mothers and offspring. In contrast, as a non-pharmacological approach against metabolic disorders, exercise is highly recommended in GDM treatment. We analysed whether gestational exercise (GE) protects mothers from diet-induced GDM metabolic consequences and mitigates liver mitochondrial deleterious alterations in their 6-week-old male offspring. Female Sprague Dawley rats were fed with control or high-fa

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Barisciano, Giovannina, Manuela Leo, Livio Muccillo, et al. "The miR-27a/FOXJ3 Axis Dysregulates Mitochondrial Homeostasis in Colorectal Cancer Cells." Cancers 13, no. 19 (2021): 4994. http://dx.doi.org/10.3390/cancers13194994.

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miR-27a plays a driver role in rewiring tumor cell metabolism. We searched for new miR-27a targets that could affect mitochondria and identified FOXJ3, an apical factor of mitochondrial biogenesis. We analyzed FOXJ3 levels in an in vitro cell model system that was genetically modified for miR-27a expression and validated it as an miR-27a target. We showed that the miR-27a/FOXJ3 axis down-modulates mitochondrial biogenesis and other key members of the pathway, implying multiple levels of control. As assessed by specific markers, the miR-27a/FOXJ3 axis also dysregulates mitochondrial dynamics, r

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Saleem, Ayesha, Heather N. Carter, and David A. Hood. "p53 is necessary for the adaptive changes in cellular milieu subsequent to an acute bout of endurance exercise." American Journal of Physiology-Cell Physiology 306, no. 3 (2014): C241—C249. http://dx.doi.org/10.1152/ajpcell.00270.2013.

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An acute bout of exercise activates downstream signaling cascades that ultimately result in mitochondrial biogenesis. In addition to inducing mitochondrial synthesis, exercise triggers the removal of damaged cellular material via autophagy and of dysfunctional mitochondria through mitophagy. Here, we investigated the necessity of p53 to the changes that transpire within the muscle upon an imposed metabolic and physiological challenge, such as a bout of endurance exercise. We randomly assigned wild-type (WT) and p53 knockout (KO) mice to control, acute exercise (AE; 90 min at 15 m/min), and AE

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Andric, Silvana, Aleksandra Markovic, Mirko Milosevic, et al. "4249 Markers of mitochondrial biogenesis, fusion and architecture are disturbed in PBMC from war veterans with posttraumatic stress disorder (PTSD)." Journal of Clinical and Translational Science 4, s1 (2020): 98–99. http://dx.doi.org/10.1017/cts.2020.307.

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OBJECTIVES/GOALS: The aim of this study was to define the transcription profiles of the molecular markers of mitochondrial biogenesis and fusion/architecture, and the markers of mtDNA copy numbers in the peripheral blood mononuclear cells (PBMCs) from war veterans with/without post-traumatic stress disorder (PTSD). METHODS/STUDY POPULATION: The peripheral blood mononuclear cells (PBMCs) from war veterans with/without post-traumatic stress disorder (PTSD) were used to monitor transcription profile of the molecular markers of mitochondrial biogenesis and fusion/architecture, as well as the marke

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Capllonch-Amer, Gabriela, Isabel Lladó, Ana M. Proenza, Francisco J. García-Palmer та Magdalena Gianotti. "Opposite effects of 17-β estradiol and testosterone on mitochondrial biogenesis and adiponectin synthesis in white adipocytes". Journal of Molecular Endocrinology 52, № 2 (2014): 203–14. http://dx.doi.org/10.1530/jme-13-0201.

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Sexual dimorphism has been found in both mitochondrial functionality and adiponectin expression in white adipose tissue, with female rats presenting more functional mitochondria than males and greater adiponectin expression. However, little is known about the role of sex hormones in this dimorphism. The aim was to elucidate the role of sex hormones in mitochondrial biogenesis and dynamics and in adiponectin synthesis in white adipocytes, and also to provide new evidence of the link between these processes. 3T3-L1 preadipocytes were differentiated and treated either with 17-β estradiol (E2; 10

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Starovlah, M. Isidora, M. Sava Radovic, A. Maja Marinovic, S. Tatjana Kostic, and A. Silvana Andric. "Psychophysical stress disturbs expression of mitochondrial biogenesis markers in hypothalamus and adenohypophysis." Biologia Serbica 39, no. 2 (2017): 43–51. https://doi.org/10.5281/zenodo.1068961.

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<strong>Summary.</strong> Although psychophysical stress is widespread in human society and a major contributor to a range of pathological conditions, it is not known if this form of stress regulates mitochondrial biogenesis in the hypothalamus or adenohypophysis, the main organs involved in compensatory specifc response of the organism to stress (so called “fght or flight” response). Accordingly, this study was designed to evaluate the effects of acute and repeated psychophysical stress on a profle of mitochondrial biogenesis markers in the hypothalamus and adenohypophysis. Rats w

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Cho, Yeong-Hyun, Ji-Young Lee, and Tae-Beom Seo. "Effects of Exercise Sequence and Circadian Rhythms on Molecular Mechanisms of Muscle Hypertrophy and Mitochondrial Biogenesis in Obese Rat." Exercise Science 32, no. 3 (2023): 347–53. http://dx.doi.org/10.15857/ksep.2023.00367.

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PURPOSE: This study aimed to investigate whether endurance and resistance training sequences and circadian rhythms affect muscle hypertrophy and mitochondrial biogenesis-related molecules in obese rats.METHODS: Rats were randomly divided into five groups: the obesity control group (OCG), aerobic-resistance exercise in the morning group (ARMG), resistance-aerobic exercise in the morning group (RAMG), aerobic resistance exercise in the evening group (AREG), and resistance-aerobic exercise in the evening group (RAEG). The exercise groups performed endurance and resistance exercises for 8 weeks ac

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Laker, Rhianna C., Mary E. Wlodek, Glenn D. Wadley, Linda A. Gallo, Peter J. Meikle та Glenn K. McConell. "Exercise early in life in rats born small does not normalize reductions in skeletal muscle PGC-1α in adulthood". American Journal of Physiology-Endocrinology and Metabolism 302, № 10 (2012): E1221—E1230. http://dx.doi.org/10.1152/ajpendo.00583.2011.

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We have previously shown that 4 wk of exercise training early in life normalizes the otherwise greatly reduced pancreatic β-cell mass in adult male rats born small. The aim of the current study was to determine whether a similar normalization in adulthood of reduced skeletal muscle mitochondrial biogenesis markers and alterations in skeletal muscle lipids of growth-restricted male rats occurs following early exercise training. Bilateral uterine vessel ligation performed on day 18 of gestation resulted in Restricted offspring born small ( P < 0.05) compared with both sham-operated Controls a

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Theilen, Nicholas T., Nevena Jeremic, Gregory J. Weber, and Suresh C. Tyagi. "Exercise preconditioning diminishes skeletal muscle atrophy after hindlimb suspension in mice." Journal of Applied Physiology 125, no. 4 (2018): 999–1010. http://dx.doi.org/10.1152/japplphysiol.00137.2018.

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The aim of the present study was to investigate whether short-term, concurrent exercise training before hindlimb suspension (HLS) prevents or diminishes both soleus and gastrocnemius atrophy and to analyze whether changes in mitochondrial molecular markers were associated. Male C57BL/6 mice were assigned to control at 13 ± 1 wk of age, 7-day HLS at 12 ± 1 wk of age (HLS), 2 wk of exercise training before 7-day HLS at 10 ± 1 wk of age (Ex+HLS), and 2 wk of exercise training at 11 ± 1 wk of age (Ex) groups. HLS resulted in a 27.1% and 21.5% decrease in soleus and gastrocnemius muscle weight-to-b

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Nesterova, V. V., P. I. Babenkova, A. A. Brezgunova, et al. "Differences in the Effects of Beta-Hydroxybutyrate on Mitochondria Biogenesis, Markers of Oxidative Stress and Inflammation in Young and Old Rat Tissues." Biohimiâ 89, no. 7 (2024): 1288–303. https://doi.org/10.31857/s0320972524070113.

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One of the therapeutic approaches to age-related diseases is to affect the metabolism of the body’s cells through certain diets or their pharmacological mimetics. The ketogenic diet significantly affects the energy metabolism of cells and the functioning of mitochondria, which is being actively studied in various age-related pathologies. In this study, we investigated the effect of the ketogenic diet mimetic beta-hydroxybutyrate (BHB) on the gene expression of proteins regulating mitochondrial biogenesis (Ppargc1a, Nrf1, Tfam), quality control (Sqstm1), the work of the antioxidant system (Nfe2

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Assayag, Miri, Ann Saada, Gary Gerstenblith, Haifa Canaana, Rivka Shlomai, and Michal Horowitz. "Mitochondrial performance in heat acclimation—a lesson from ischemia/reperfusion and calcium overload insults in the heart." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 8 (2012): R870—R881. http://dx.doi.org/10.1152/ajpregu.00155.2012.

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Long-term heat acclimation (LTHA; 30 days, 34°C) causes phenotypic adaptations that render protection against ischemic/reperfusion insult (I/R, 30 min global ischemia and 40 min reperfusion) via heat acclimation-mediated cross-tolerance (HACT) mechanisms. Short-term acclimation (STHA, 2 days, 34°C), in contrast, is characterized by cellular perturbations, leading to increased susceptibility to insults. Here, we tested the hypothesis that enhanced mitochondrial respiratory function is part of the acclimatory repertoire and that the 30-day regimen is required for protection via HACT. We subjecte

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Stevens, Daniel A., Yunjong Lee, Ho Chul Kang, et al. "Parkin loss leads to PARIS-dependent declines in mitochondrial mass and respiration." Proceedings of the National Academy of Sciences 112, no. 37 (2015): 11696–701. http://dx.doi.org/10.1073/pnas.1500624112.

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Mutations in parkin lead to early-onset autosomal recessive Parkinson’s disease (PD) and inactivation of parkin is thought to contribute to sporadic PD. Adult knockout of parkin in the ventral midbrain of mice leads to an age-dependent loss of dopamine neurons that is dependent on the accumulation of parkin interacting substrate (PARIS), zinc finger protein 746 (ZNF746), and its transcriptional repression of PGC-1α. Here we show that adult knockout of parkin in mouse ventral midbrain leads to decreases in mitochondrial size, number, and protein markers consistent with a defect in mitochondrial

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Li, Cong, Xiao Yan Ding, Dong Mei Xiang, et al. "Enhanced M1 and Impaired M2 Macrophage Polarization and Reduced Mitochondrial Biogenesis via Inhibition of AMP Kinase in Chronic Kidney Disease." Cellular Physiology and Biochemistry 36, no. 1 (2015): 358–72. http://dx.doi.org/10.1159/000430106.

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Background: Macrophage polarization plays a pivotal role in the process of inflammation which is common in chronic kidney disease (CKD). Macrophages polarization under the condition of CKD remains poorly understood. Here we tested the hypothesis that CKD promotes macrophage M1 polarization. Methods: A rat model of CKD was established by reduced renal mass (RRM). Polarization of macrophages was induced in ex vivo macrophages from RRM rats and cultured ones under the condition of uremic serum. The markers were evaluated by RT-PCR, western blot, and flow cytometer. Results: Our data showed that m

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Khashchenko, Elena P., Mikhail Yu Vysokikh, Maria V. Marey, et al. "Altered Glycolysis, Mitochondrial Biogenesis, Autophagy and Apoptosis in Peritoneal Endometriosis in Adolescents." International Journal of Molecular Sciences 25, no. 8 (2024): 4238. http://dx.doi.org/10.3390/ijms25084238.

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Energy metabolism plays a pivotal role in the pathogenesis of endometriosis. For the initial stages of the disease in adolescents, this aspect remains unexplored. The objective of this paper was to analyze the association of cellular and endosomal profiles of markers of glycolysis, mitochondrial biogenesis, apoptosis, autophagy and estrogen signaling in peritoneal endometriosis (PE) in adolescents. We included 60 girls aged 13–17 years in a case–control study: 45 with laparoscopically confirmed PE (main group) and 15 with paramesonephric cysts (comparison group). Samples of plasma and peritone

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Silva, Joana V., Joana Santiago, Bárbara Matos, et al. "Effects of Age and Lifelong Moderate-Intensity Exercise Training on Rats’ Testicular Function." International Journal of Molecular Sciences 23, no. 19 (2022): 11619. http://dx.doi.org/10.3390/ijms231911619.

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Aging is associated with testicular morphological and functional alterations, but the underlying molecular mechanisms and the impact of physical exercise are poorly understood. In this study, we examined the effects of age and lifelong moderate-intensity exercise on rat testis. Mature adults (35 weeks) and middle-aged (61 weeks) Wistar Unilever male rats were maintained as sedentary or subjected to a lifelong moderate-intensity treadmill training protocol. Testis weight and histology, mitochondrial biogenesis and function, and proteins involved in protein synthesis and stress response were eva

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Steiner, Jennifer L., E. Angela Murphy, Jamie L. McClellan, Martin D. Carmichael, and J. Mark Davis. "Exercise training increases mitochondrial biogenesis in the brain." Journal of Applied Physiology 111, no. 4 (2011): 1066–71. http://dx.doi.org/10.1152/japplphysiol.00343.2011.

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Increased muscle mitochondria are largely responsible for the increased resistance to fatigue and health benefits ascribed to exercise training. However, very little attention has been given to the likely benefits of increased brain mitochondria in this regard. We examined the effects of exercise training on markers of both brain and muscle mitochondrial biogenesis in relation to endurance capacity assessed by a treadmill run to fatigue (RTF) in mice. Male ICR mice were assigned to exercise (EX) or sedentary (SED) conditions ( n = 16–19/group). EX mice performed 8 wk of treadmill running for 1

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Mannam, Praveen, Amanda S. Shinn, Anup Srivastava, et al. "MKK3 regulates mitochondrial biogenesis and mitophagy in sepsis-induced lung injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 306, no. 7 (2014): L604—L619. http://dx.doi.org/10.1152/ajplung.00272.2013.

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Sepsis is a systemic inflammatory response to infection and a major cause of death worldwide. Because specific therapies to treat sepsis are limited, and underlying pathogenesis is unclear, current medical care remains purely supportive. Therefore targeted therapies to treat sepsis need to be developed. Although an important mediator of sepsis is thought to be mitochondrial dysfunction, the underlying molecular mechanism is unclear. Modulation of mitochondrial processes may be an effective therapeutic strategy in sepsis. Here, we investigated the role of the kinase MKK3 in regulation of mitoch

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Liu, Meihong, Mingzhu Zheng, Dan Cai та ін. "Zeaxanthin promotes mitochondrial biogenesis and adipocyte browning via AMPKα1 activation". Food & Function 10, № 4 (2019): 2221–33. http://dx.doi.org/10.1039/c8fo02527d.

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Dayanidhi, Sudarshan. "SKELETAL MUSCLE MITOCHONDRIAL PHYSIOLOGY IN CHILDREN WITH CEREBRAL PALSY: CONSIDERATIONS FOR HEALTHY AGING." Innovation in Aging 6, Supplement_1 (2022): 129. http://dx.doi.org/10.1093/geroni/igac059.516.

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Abstract During healthy aging, there is an overall decline in mitochondrial activity and abundance, increase in mitochondrial DNA mutations, increase in oxidative stress, and reduction in overall muscular capacity. Individuals with cerebral palsy (CP) have significantly increased energetics of movement, reduced endurance capacity, and increased perceived effort. We will cover the results of recent work in muscles in ambulatory children with CP that show a marked reduction in mitochondrial function. Muscles show that mitochondrial protein content and DNA copy number are lower, suggesting a redu

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Petersson, Stine J., Louise L. Christensen, Jonas M. Kristensen, Rikke Kruse, Marianne Andersen, and Kurt Højlund. "Effect of testosterone on markers of mitochondrial oxidative phosphorylation and lipid metabolism in muscle of aging men with subnormal bioavailable testosterone." European Journal of Endocrinology 171, no. 1 (2014): 77–88. http://dx.doi.org/10.1530/eje-14-0006.

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ObjectiveRecent studies have indicated that serum testosterone in aging men is associated with insulin sensitivity and expression of genes involved in oxidative phosphorylation (OxPhos), and that testosterone treatment increases lipid oxidation. Herein, we investigated the effect of testosterone therapy on regulators of mitochondrial biogenesis and markers of OxPhos and lipid metabolism in the skeletal muscle of aging men with subnormal bioavailable testosterone levels.MethodsSkeletal muscle biopsies were obtained before and after treatment with either testosterone gel (n=12) or placebo (n=13)

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Granata, Cesare, Rodrigo S. F. Oliveira, Jonathan P. Little та David J. Bishop. "Forty high-intensity interval training sessions blunt exercise-induced changes in the nuclear protein content of PGC-1α and p53 in human skeletal muscle". American Journal of Physiology-Endocrinology and Metabolism 318, № 2 (2020): E224—E236. http://dx.doi.org/10.1152/ajpendo.00233.2019.

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Exercise-induced increases in peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) and p53 protein content in the nucleus mediate the initial phase of exercise-induced mitochondrial biogenesis. Here, we investigated whether exercise-induced increases in these and other markers of mitochondrial biogenesis were altered after 40 sessions of twice-daily high-volume, high-intensity interval training (HVT) in human skeletal muscle. Vastus lateralis muscle biopsies were collected from 10 healthy recreationally active participants before, immediately postexercise, and 3 h after a sessi

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Manfredini, Andressa, Larissa Constantino, Milton Castro Pinto, et al. "Mitochondrial dysfunction is associated with long-term cognitive impairment in an animal sepsis model." Clinical Science 133, no. 18 (2019): 1993–2004. http://dx.doi.org/10.1042/cs20190351.

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Abstract Background: Several different mechanisms have been proposed to explain long-term cognitive impairment in sepsis survivors. The role of persisting mitochondrial dysfunction is not known. We thus sought to determine whether stimulation of mitochondrial dynamics improves mitochondrial function and long-term cognitive impairment in an experimental model of sepsis. Methods: Sepsis was induced in adult Wistar rats by cecal ligation and perforation (CLP). Animals received intracerebroventricular injections of either rosiglitazone (biogenesis activator), rilmenidine, rapamycin (autophagy acti

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Bhogoju, Sarayu, Neeraj Kapur, Hemendra Vekaria, et al. "ENHANCED MITOCHONDRIAL BIOGENESIS INCREASES ANTI-OXIDANT ENZYMES AND IMPROVES TISSUE INFLAMMATION IN HUMAN IBD TISSUE." Inflammatory Bowel Diseases 30, Supplement_1 (2024): S58—S59. http://dx.doi.org/10.1093/ibd/izae020.119.

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Abstract BACKGROUND In patients with inflammatory bowel disease (IBD), there exists a connection between mitochondrial dysfunction and two key issues: increased oxidative stress and attenuated ATP production. Previously we presented at this meeting the effect of a novel gold-based compound (AuPhos) on enhancing mitochondrial function in attenuating mice colitis (). In the present study we interrogate the effect of AuPhos on mitochondrial biogenesis in biopsies from control and active ulcerative colitis (UC) (Mayo 1-2) patients and normal human colonic epithelial cells (NCM460). We postulate th

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Herath, Sanjeeva, Amy Y. M. Au, Kylie M. Taylor, Natasha Kapoor-Kaushik, Zoltán H. Endre, and Jonathan H. Erlich. "Long-Term Functional and Structural Renoprotection After Experimental Acute Kidney Injury in Subclinical Chronic Kidney Disease In Vivo." International Journal of Molecular Sciences 26, no. 10 (2025): 4616. https://doi.org/10.3390/ijms26104616.

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Subclinical chronic kidney disease (sCKD) predisposes one to acute kidney injury (AKI) and chronic kidney disease (CKD). Reduced kidney functional reserve (KFR) detects sCKD in preclinical studies and predicts AKI after cardiac surgery. We evaluated renal protection in a rat model of kidney injury where ischaemia–reperfusion injury (IRI) was induced after sCKD. Dual treatment boosting nicotinamide adenine dinucleotide (NAD) by nicotinamide riboside (NR) combined with the mitochondria-targeted antioxidant SkQR1 protected the KFR and reduced structural kidney damage, including markers of vascula

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Latino, Debora, Massimo Venditti, Sara Falvo, et al. "Steroidogenesis Upregulation through Mitochondria-Associated Endoplasmic Reticulum Membranes and Mitochondrial Dynamics in Rat Testes: The Role of D-Aspartate." Cells 13, no. 6 (2024): 523. http://dx.doi.org/10.3390/cells13060523.

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Mitochondria-Associated Endoplasmic Reticulum Membranes (MAMs) mediate the communication between the Endoplasmic Reticulum (ER) and the mitochondria, playing a fundamental role in steroidogenesis. This study aimed to understand how D-aspartate (D-Asp), a well-known stimulator of testosterone biosynthesis and spermatogenesis, affects the mechanism of steroidogenesis in rat testes. Our results suggested that D-Asp exerts this function through MAMs, affecting lipid trafficking, calcium signaling, ER stress, and mitochondrial dynamics. After 15 days of oral administration of D-Asp to rats, there w

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Ho, Jou-Hsuan, Rathinasamy Baskaran, Ming-Fu Wang та ін. "Bioactive Peptides and Exercise Modulate the AMPK/SIRT1/PGC-1α/FOXO3 Pathway as a Therapeutic Approach for Hypertensive Rats". Pharmaceuticals 15, № 7 (2022): 819. http://dx.doi.org/10.3390/ph15070819.

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Peptides are fragments of fundamental protein sequences that may have health benefits in addition to basic dietary benefits. Recently, we have reported on the pharmacological benefits of alcalase potato protein hydrolysate (APPH) and bioactive peptides isolated from APPH. The aim was to evaluate the synergistic effect of exercise along with DIKTNKPVIF (DF) peptides in ameliorating hypertension in spontaneously hypertensive rat (SHR) rats. We examined ECG parameters, lipid profiles, cardiac markers, and histology, and quantified the proteins associated with fibrosis, hypertrophy, apoptosis, mit

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Hafez, Hala A., Ali M. Atoom, Rana H. M. Khafaga, et al. "Direct-Acting Antiviral Drug Modulates the Mitochondrial Biogenesis in Different Tissues of Young Female Rats." International Journal of Molecular Sciences 24, no. 21 (2023): 15844. http://dx.doi.org/10.3390/ijms242115844.

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(1) Background: Hepatitis C virus (HCV) infection is endemic in Egypt, with the highest prevalence rate worldwide. Sofosbuvir (SOF) is a nucleos(t)ide analog that specifically inhibits HCV replication. This study aimed to explore the possible effects of the therapeutic dose of SOF on the mitochondrial biogenesis and functions of the liver, muscle, and ovarian tissues of young normal female rats. (2) Methods: This study was conducted on 20 female Wistar rats, classified into two groups, the control group and the exposed group; the latter was orally supplemented with 4 mg/kg/day of SOF for 3 mon

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Bhogoju, Sarayu, Neeraj Kapur, Luksana Chaiswing, et al. "A NOVEL DRUG THERAPY INDUCES MITOCHONDRIAL BIOGENESIS AND ATTENUATES COLITIS." Inflammatory Bowel Diseases 29, Supplement_1 (2023): S55. http://dx.doi.org/10.1093/ibd/izac247.106.

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Abstract Mitochondrial dysfunction is a characteristic feature of intestinal epithelium cells (IEC) in IBD patients, associated with oxidative stress and impaired ATP production. We posit that disrupted mitochondrial bioenergetics impairs ulcer healing in IBD. In the current study, we tested a novel gold-based compound (AuPhos) that improves mitochondrial function by increasing mitochondrial biogenesis and antioxidant enzymes in IEC and human colonic biopsies. METHODS: Normal human colonic epithelial cells (NCM460) were used to evaluate the effect of AuPhos on mitochondrial proteins and anti-o

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Miller, Colette, Janaiya Samuels, Yusra Azhar, Ashish Parmar, Rangaiah Shashidharamurthy, and Srujana Rayalam. "Guggulsterone Activates Adipocyte Beiging through Direct Effects on 3T3-L1 Adipocytes and Indirect Effects Mediated through RAW264.7 Macrophages." Medicines 6, no. 1 (2019): 22. http://dx.doi.org/10.3390/medicines6010022.

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Background: Plant-derived phytochemicals have been of emerging interest as anti-obesity compounds due to their apparent effects on promoting reduced lipid accumulation in adipocytes. Despite such promising evidence, little is known about the potential mechanisms behind their anti-obesity effects. The aim of this study is to establish potential anti-obesity effects of the phytochemical guggulsterone (GS). Methods: Mature 3T3-L1 adipocytes were treated with GS, derived from the guggul plant native in northern India, to investigate its effects on mitochondrial biogenesis and adipocyte “beiging.”

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Robinson, Matthew M., Jennifer C. Richards, Matthew S. Hickey та ін. "Acute β-adrenergic stimulation does not alter mitochondrial protein synthesis or markers of mitochondrial biogenesis in adult men". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, № 1 (2010): R25—R33. http://dx.doi.org/10.1152/ajpregu.00524.2009.

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Exercise-induced expression of peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) is dramatically inhibited in mice pretreated with a β-adrenergic receptor (β-AR) antagonist, suggesting that β-ARs play an important role in the regulation of skeletal muscle PGC-1α expression, and potentially, mitochondrial biogenesis. Accordingly, we hypothesized that acute β-AR stimulation would induce transcriptional pathways involved in skeletal muscle mitochondrial biogenesis in humans. Whole body protein turnover (WBPT), myofibrillar protein synthesis (MyPS), skeletal muscle mitochond

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Lee, Harold W., Ella Baker, Kevin M. Lee, Aaron M. Persinger, William Hawkins, and Melissa Puppa. "Effects of low-dose leucine supplementation on gastrocnemius muscle mitochondrial content and protein turnover in tumor-bearing mice." Applied Physiology, Nutrition, and Metabolism 44, no. 9 (2019): 997–1004. http://dx.doi.org/10.1139/apnm-2018-0765.

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Many forms of cancer are associated with loss of lean body mass, commonly attributed to decreased protein synthesis and stimulation of proteolytic pathways within the skeletal muscle. Leucine has been shown to improve protein synthesis, insulin signaling, and mitochondrial biogenesis, which are key signaling pathways influenced by tumor signaling. The purpose of this study was to examine the effects of leucine supplementation on mitochondrial biogenesis and protein turnover in tumor-bearing mice. Twenty male C57BL/6 mice were divided into 4 groups (n = 5): Chow, leucine (Leu), Lewis lung carci

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Davis, J. Mark, E. Angela Murphy, Martin D. Carmichael, and Ben Davis. "Quercetin increases brain and muscle mitochondrial biogenesis and exercise tolerance." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 4 (2009): R1071—R1077. http://dx.doi.org/10.1152/ajpregu.90925.2008.

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Quercetin is one of a broad group of natural polyphenolic flavonoid substances that are being investigated for their widespread health benefits. These benefits have generally been ascribed to its combination of antioxidant and anti-inflammatory activity, but recent in vitro evidence suggests that improved mitochondrial biogenesis could play an important role. In addition, the in vivo effects of quercetin on mitochondrial biogenesis exercise tolerance are unknown. We examined the effects of 7 days of quercetin feedings in mice on markers of mitochondrial biogenesis in skeletal muscle and brain,

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Carter, Heather N., and David A. Hood. "Contractile activity-induced mitochondrial biogenesis and mTORC1." American Journal of Physiology-Cell Physiology 303, no. 5 (2012): C540—C547. http://dx.doi.org/10.1152/ajpcell.00156.2012.

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In response to exercise training, or chronic contractile activity, mitochondrial content is known to be enriched within skeletal muscle. However, the molecular mechanisms that mediate this adaptation are incompletely defined. Recently, the protein complex, mammalian target of rapamycin complex 1 (mTORC1), has been identified to facilitate the expression of nuclear genes encoding mitochondrial proteins (NUGEMPs) in resting muscle cells via the interaction of the mTORC1 components, mTOR and raptor, the transcription factor Yin Yang 1, and peroxisome proliferator-activated receptor-γ coactivator-

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Balogun, Kayode, and Lena Serghides. "Comparison of the Effects of Three Dual-Nucleos(t)ide Reverse Transcriptase Inhibitor Backbones on Placenta Mitochondria Toxicity and Oxidative Stress Using a Mouse Pregnancy Model." Pharmaceutics 14, no. 5 (2022): 1063. http://dx.doi.org/10.3390/pharmaceutics14051063.

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Nucleos(t)ide reverse transcriptase inhibitors (NRTIs) are the backbone of HIV antiretroviral therapy (ART). ART use in pregnancy has been associated with adverse birth outcomes, in part due to NRTI-induced mitochondrial toxicity. Direct comparison on the effects of commonly used dual-NRTI regimens on placental mitochondria toxicity in pregnancy is lacking. We compared zidovudine/lamivudine, abacavir/lamivudine, and tenofovir/emtricitabine using a mouse model and examined markers of placental mitochondrial function and oxidative stress. Zidovudine/lamivudine and abacavir/lamivudine were associ

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Hadsell, Darryl L., Walter Olea, Jerry Wei, et al. "Developmental regulation of mitochondrial biogenesis and function in the mouse mammary gland during a prolonged lactation cycle." Physiological Genomics 43, no. 6 (2011): 271–85. http://dx.doi.org/10.1152/physiolgenomics.00133.2010.

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The regulation of mitochondrial biogenesis and function in the lactating mammary cell is poorly understood. The goal of this study was to use proteomics to relate temporal changes in mammary cell mitochondrial function during lactation to changes in the proteins that make up this organelle. The hypothesis tested was that changes in mammary cell mitochondrial biogenesis and function during lactation would be accounted for by coordinated changes in the proteins of the electron transport chain and that some of these proteins might be linked by their expression patterns to PPARGC1α and AMP kinase.

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Aimaretti, Eleonora, Guglielmina Chimienti, Chiara Rubeo, et al. "Different Effects of High-Fat/High-Sucrose and High-Fructose Diets on Advanced Glycation End-Product Accumulation and on Mitochondrial Involvement in Heart and Skeletal Muscle in Mice." Nutrients 15, no. 23 (2023): 4874. http://dx.doi.org/10.3390/nu15234874.

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Diets with an elevated content of fat, sucrose, or fructose are recognized models of diet-induced metabolic alterations, since they induce metabolic derangements, oxidative stress, and chronic low-grade inflammation associated with local and systemic accumulation of advanced glycation end-products (AGEs). This study used four-week-old C57BL/6 male mice, randomly assigned to three experimental dietary regimens: standard diet (SD), high-fat high-sucrose diet (HFHS), or high fructose diet (HFr), administered for 12 weeks. Plasma, heart, and tibialis anterior (TA) skeletal muscle were assayed for

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Patyal, Pankaj, Gohar Azhar, Ambika Verma, Xiaomin Zhang, and Jeanne Y. Wei. "CARDIAC SPECIFIC OVEREXPRESSION OF SERUM RESPONSE FACTOR ALTERS MITOCHONDRIAL STRUCTURE AND FUNCTION." Innovation in Aging 8, Supplement_1 (2024): 1135. https://doi.org/10.1093/geroni/igae098.3640.

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Abstract Serum response factor (SRF) is a transcription factor required for the regulation of genes important for cardiac structure and function. Previously, we have shown that increased levels of SRF in transgenic mouse carrying human SRF under Myh6 promoter resulted in cardiomyopathy and early mortality. Although, there is a rapidly growing body of literature investigating the effects of aging on the heart and how age-related alterations affect cardiac and mitochondrial function, and underlying mechanisms remain unclear. Herein, we tested the hypothesis whether cardiac specific overexpressio

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Mekala, Naveen, Jacob Kurdys, Alexis Paige Vicenzi, et al. "MiR 208a Regulates Mitochondrial Biogenesis in Metabolically Challenged Cardiomyocytes." Cells 10, no. 11 (2021): 3152. http://dx.doi.org/10.3390/cells10113152.

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Metabolic syndrome increases the risk for cardiovascular disease including metabolic cardiomyopathy that may progress to heart failure. The decline in mitochondrial metabolism is considered a critical pathogenic mechanism that drives this progression. Considering its cardiac specificity, we hypothesized that miR 208a regulates the bioenergetic metabolism in human cardiomyocytes exposed to metabolic challenges. We screened in silico for potential miR 208a targets focusing on mitochondrial outcomes, and we found that mRNA species for mediator complex subunit 7, mitochondrial ribosomal protein 28

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Mumford, Petey W., Shelby C. Osburn, Carlton D. Fox, Joshua S. Godwin, and Michael D. Roberts. "A Theacrine-Based Supplement Increases Cellular NAD+ Levels and Affects Biomarkers Related to Sirtuin Activity in C2C12 Muscle Cells In Vitro." Nutrients 12, no. 12 (2020): 3727. http://dx.doi.org/10.3390/nu12123727.

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There is evidence in rodents to suggest that theacrine-based supplements modulate tissue sirtuin activity as well as other biological processes associated with aging. Herein, we examined if a theacrine-based supplement (termed NAD3) altered sirtuin activity in vitro while also affecting markers of mitochondrial biogenesis. The murine C2C12 myoblast cell line was used for experimentation. Following 7 days of differentiation, myotubes were treated with 0.45 mg/mL of NAD3 (containing ~2 mM theacrine) for 3 and 24 h (n = 6 treatment wells per time point). Relative to control (CTL)-treated cells, N

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